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This Article Full Text Full Text (PDF) All Versions of this Article: 292/5/H2285    most recent 00981.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Gonzalez, N. C. Articles by Wood, J. G. Search for Related Content PubMed PubMed Citation Articles by Gonzalez, N. C. Articles by Wood, J. G.

Role of the renin-angiotensin system in the systemic microvascular inflammation of alveolar hypoxia

Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas

Submitted 8 September 2006 ; accepted in final form 4 January 2007

Alveolar hypoxia (AH) induces widespread systemic inflammation. Previous studies have shown dissociation between microvascular PO₂ and inflammation. Furthermore, plasma from AH rats (PAHR) induces mast cell (MC) activation, inflammation, and vasoconstriction in normoxic cremasters, while plasma from normoxic rats does not produce these responses. These results suggest that inflammation of AH is triggered by a blood-carried agent. This study investigated the involvement of the renin-angiotensin system (RAS) in the inflammation of AH. Both an angiotensin-converting enzyme (ACE) inhibitor and an angiotensin II (ANG II) receptor blocker (ANG II RB) inhibited the leukocyte-endothelial adherence produced by AH, as well as the inflammation produced by PAHR in normoxic rat cremasters. MC stabilization with cromolyn blocked the effects of PAHR but not those of topical ANG II on normoxic cremasters, suggesting ANG II generation via MC activation by PAHR. This was supported by the observation that ACE inhibition and ANG II RB blocked the leukocyte-endothelial adherence produced by the MC secretagogue compound 48/80. These results suggest that the intermediary agent contained in PAHR activates MC and stimulates the RAS, leading to inflammation, and imply an RAS role in AH-induced inflammation.

microcirculation; mast cells

This article has been cited by other articles:

				N. C. Gonzalez, J. Allen, V. G. Blanco, E. J. Schmidt, N. van Rooijen, and J. G. Wood Alveolar macrophages are necessary for the systemic inflammation of acute alveolar hypoxia J Appl Physiol, October 1, 2007; 103(4): 1386 - 1394. [Abstract] [Full Text] [PDF]